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Influence of R-type (Cav2.3) and t-type (Cav3.1-3.3) antagonists on nigral somatodendritic dopamine release measured by microdialysis.

Journal article
Authors Filip Bergquist
Hans Nissbrandt
Published in Neuroscience
Volume 120
Issue 3
Pages 757-64
ISSN 0306-4522
Publication year 2003
Published at Institute of Physiology and Pharmacology, Dept of Pharmacology
Pages 757-64
Language en
Keywords 3,4-Dihydroxyphenylacetic Acid, metabolism, Animals, Calcium Channel Blockers, pharmacology, Calcium Channels, R-Type, metabolism, Calcium Channels, T-Type, metabolism, Dendrites, drug effects, metabolism, Dopamine, metabolism, secretion, Homovanillic Acid, metabolism, Male, Microdialysis, Rats, Rats, Sprague-Dawley, Substantia Nigra, drug effects, metabolism
Subject categories Physiology


The release of dopamine from soma and dendrites of dopaminergic neurons in substantia nigra has been reported to be calcium-dependent, but it remains to be determined which calcium channels mediate this effect. We have used in vivo microdialysis in rat substantia nigra and striatum to investigate the effect of Ca(v)3.1-3.3 (T-type) and Ca(v)2.3 (R-type) calcium channel antagonists on somatodendritic and terminal dopamine release. Local reverse dialysis administration of 0.1-10 microM of the Ca(v)2.3 inhibitor SNX-482, or 100 microM of mibefradil, decreased the concentrations of dopamine and its metabolites in dialysate from substantia nigra, whereas 1 microM mibefradil or 40-80 microM nickel(II) induced an increase in nigral dialysate dopamine concentrations. Dopamine concentrations in striatal dialysates were decreased only by 10 microM of SNX-482 or 100 microM of mibefradil. Nickel(II) induced an increase in striatal dialysate dopamine concentration similar to that in substantia nigra. The results indicate a role for Ca(v)2.3 (R-type) voltage sensitive calcium channels in the calcium dependency of somatodendritic dopamine release, but argue against a calcium dependency mediated substantially by Ca(v)3.1-3.3 (T-type) channels.

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